Vaccine development has been identified as essential to controlling infection with C. trachomatis. Vaccines against C. trachomatis appear to elicit protective T-cell and/or B-cell immunity in the genital tract mucosa.
Protective immunity to C. trachomatis seems to depend on a Th1-polarized cell-mediated immune response, in particular on CD4+ lymphocytes secreting IFNγ. For example, depletion of CD4+ T cells in mice results in loss of protective immunity, and adoptive transfer of Chlamydia-specific CD4+ T cells confers protection against challenge with C. trachomatis. Furthermore, recent studies report that C. trachomatis infection in mice induces a CD4-Th1 protective immune response, indicating that critical Chlamydia antigens are processed and presented via the MHC class II pathway (Brunham R C and Rey-Ladino J (2005), Nat Rev Immunol 5: 149-1611; Su H and Caldwell H D (1995), Infect Immun 63: 3302-3308).
Although B-cells and antibodies do not have a decisive role in resolution of primary infection, they are likely to be important for enhancing the protective effector T-cell response and to be required to control re-infection with various mechanisms such as antibody-mediated neutralization and opsonization.
Because immune protection against infection with C. trachomatis is likely to be mediated by immunization with C. trachomatis proteins that are targets of CD4+ T cells and that are capable of inducing B-cell responses, identification of such proteins is particularly important. It is therefore an object of the invention to provide further antigens for use in Chlamydia vaccines.